Dendritic cell populations in the eutopic and ectopic endometrium of women with endometriosis

Abstract

Both CD1a+ and CD83+ DC populations were altered in the eutopic and ectopic endometrium of women with endometriosis compared with controls. Alterations in these cells, which play a crucial role in the coordination of the immune response, may be involved in pain generation and the pathogenesis of endometriosis.

Molecular Cross-Talk at the Feto–Maternal Interface

“…They play a role in remodeling the cycling endometrium following through to either menstruation or implantation and are key to initiation and modulation of maternal -fetal immune responses (Bengtsson et al 2004). CD1a 2 immature dendritic cells differentiate from their precursors and become proficient at antigen detection via toll like receptors (Reis e Sousa 2001), antigen processing and presenting, thus bridging the gap between the innate and acquired immune systems (Sallusto and Lanzavecchia 1999;Schulke et al 2009). Engulfment and digestion of antigens and inflammatory cytokines induces migration of dendritic cells to lymphoid organs where they efficiently activate naïve T cells and regulate NK and B cells (Crow and Kunkel 1982;Banchereau et al 2000).…”

“…Engulfment and digestion of antigens and inflammatory cytokines induces migration of dendritic cells to lymphoid organs where they efficiently activate naïve T cells and regulate NK and B cells (Crow and Kunkel 1982;Banchereau et al 2000). Mature dendritic cells express CD83 as well as an array of costimulatory molecules such as CD40, CD58, CD80, CD86, MHC molecules, and high levels of CC-chemokine receptor (CCR)-7 (Sallusto et al 1995(Sallusto et al , 2000Cella et al 1999; Reis e Sousa 2001; Schulke et al 2009). CCR-7 stimulates dendritic cell migration to secondary lymphoid organs, where they attract and present antigens to CD4 þ and CD8 þ T cells (Sallusto et al 2000; Reis e Sousa 2001; Juretic et al 2004).…”

Immunity at the Maternal–Fetal Interface

“…They have a role in remodeling the cycling endometrium following through to either menstruation or implantation and are key to initiating and modulating maternal-fetal immune responses (Bengtsson et al, 2004). CD1a − immature DCs (iDCs) differentiate from their precursors and become proficient at antigen detection via TLRs (Reis e Sousa, 2001), antigen processing, and presenting, thus bridging the gap between the innate and acquired immune systems (Sallusto and Lanzavecchia, 1999;Schulke et al, 2009). Engulfment and digestion of antigens and inflammatory cytokines induce migration of DCs to lymphoid organs where they efficiently activate naïve T cells and regulate NK and B cells (Crow and Kunkel, 1982;Banchereau et al, 2000).…”

Pecularities of functional state of antigen-presenting cells of the endometrium in patients with deep infiltrating endometriosis

“…Зовнішній генітальний ендометріоз нале-жить до найбільш розповсюджених захворю-вань жіночої статевої системи, посідаючи тре-тє місце у структурі гінекологічної патології після запальних процесів та міоми матки [1,2]. Ризик розвитку неплідності при зовнішньому генітальному ендометріозі у пацієнток репро-дуктивного віку підвищується в 20 разів.…”